2 replies to this topic

[cargocultist]

Many people are aware that nicotine appears to substantially increase cognitive performance in some areas such as fine motor skills and increasing iq by a few points. A major downside to using nicotine is the vasoconstrictive effect it has throughout the body including the brain which could have a negative effect on cognition, depending on other physiological factors that differ between subjects. 

 

Cinnerazine is used for preventing motion sickness and has these properties:

Calcium ion channel antagonist T-type calcium channels Antihistaminic H1 receptors Antiserotinergic 5-HT₂ receptors^[37] Antidopaminergic D2 receptors

 

Cinnerazine is a t-type calcium channel blocker improving blood flow to the brain without affecting the heart: 

The mechanism of action of calcium antagonists relative to their clinical applications

→ source (external link)

Blocking t-type channels maybe useful against epilepsy (and consequently for sub-clinical neuronal hyperexcitability): 

The role of T-type calcium channels in epilepsy and pain.

→ source (external link)

Some more facts on cinnerazine side effects:

Side effects according to wikipedia (Parkinsonism et cetera)

→ source (external link)

 

Unfortunately cinnerazine and its metabolites appear to cause parkisonism by binding to D-2 dopamine receptors and blocking presynaptic uptake, counterindicating it as a long term nootropic. However, nicotine and/or cotinine seem to protect against Parkinson's by having an opposing effect on dopamine in the brain: 

Pooled Analysis of Tobacco Use and Risk of Parkinson Disease

→ source (external link)

A combo of piracetam and cinnerazine is used in Russia to treat cerebral insufficiency, supposedly synergising the effect of blood thinning and cerebro-vasodilation to support the brain. 

[Use of omaron in patients with post-stroke cognitive disorders].

→ source (external link)

 

I take half a tablet (25/2=12.5mg) cinnerazine and put half a fragmented nicotine lozenge under the tongue. Mostly often I do this in the evening. Other forms of nicotine administration, barring smoking, are obviously fine as well. The mild anticholinergic and antihistaminergic effects of cinnerazine help me sleep a little better as well. Those effects only become obvious when the energizing effect of the nicotine wears off. It's a great combo.

[Doc Psychoillogical]

Correct me if i'm wrong but Remeron(Mirtazapine) has a few of those properties.

 

Wikipedia: Investigational[edit]

Mirtazapine has had literature published on its efficacy in the experimental treatment of these conditions:

• Sleep apnoea/hypopnoea^[28][29]
• Inappropriate sexual behaviour and other secondary symptoms of autistic spectrum conditions and other pervasive developmental disorders^{[30][31][32][33]}
• Antipsychotic-induced akathisia^[34][35]
• Drug withdrawal, dependence and detoxification^[36]
• Negative, depressive and cognitive symptoms of schizophrenia (as an adjunct)^[37][38]
• A case report has been published in which mirtazapine reduced visual hallucinations in a patient with Parkinson's diseasepsychosis (PDP).^[39] This is in alignment with recent findings that inverse agonists at the 5-HT_2A receptors are efficacious in attenuating the symptoms of Parkinson's disease psychosis. As is supported by the common practice of prescribing low-dosequetiapine and clozapine for PDP—doses too low to antagonise the D₂ receptor, but sufficiently high doses to inversely agonise the 5-HT_2A receptors.^[40]

 

 

Molecular target Binding affinity, K_i(nM)^[71] Notes 5-HT_2A receptor 69 The (S)-(+) enantiomer is responsible for this antagonism.^[6] 5-HT_2B receptor  ? ~20-fold lower than for 5-HT_2A/5-HT_2C^[72] 5-HT_2C receptor 39 Inverse agonist^[73] The (S)-(+) enantiomer is responsible for this action.^[6] 5-HT₃ receptor  ? Similar to 5-HT_2A/5-HT_2C (mouse neuroblastoma cell)^[74] R-(–) enantiomer antagonises the 5-HT₃ receptor.^[6] 5-HT₇ receptor 265   α₁-adrenergic receptor 500 ^[75] α_2A-adrenergic receptor 20 The S-(+) enantiomer is responsible for this antagonism at autoreceptors.^[6] Heteroreceptors are blocked by both the (S)-(+) and (R)-(–) enantiomers.^[3] α_2C-adrenergic receptor 18 The S-(+) enantiomer is responsible for this antagonism at autoreceptors.^[6] Heteroreceptors are blocked by both the (S)-(+) and (R)-(–) enantiomers.^[3] D₁ receptor 4167   D₂ receptor >5454   D₃ receptor 5723   H₁ receptor 1.6 ^[76] mACh receptors 670 ^[75]

All affinities listed were assayed using human materials except those for α₁-adrenergic and mACh that are for rat tissues, due to human values being unavailable.^[69][70]

Mirtazapine has recently been found to act as a weak (EC₅₀ 7.2 μM) κ-opioid receptor partial agonist.^[77]

[cargocultist]

Correct me if i'm wrong but Remeron(Mirtazapine) has a few of those properties.

 

.......

Not really and you're polluting my thread.

 

My first basic point is that nicotine can be made more effective by counteracting it's cerebro-vasoconstricting effect with the t-type calcium channel blocker cinnerazine. A particular benefit to using a t-type CCB is that it's pretty much brain selective. That and a possible benefit of its supposed anti-epileptic effect. 

 

My second basic point is that nicotine may prevent the dangerous side effect of induced parkinsonism associated with cinnerazine use.